{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Desdin-Mico G"],"funding":["Juan de la Cierva","European Research Council","Atracción de Talento Investigador Grant","Fondo de Investigación Sanitaria del Instituto de Salud Carlos III"],"pagination":["1371-1376"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7616968"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["368(6497)"],"pubmed_abstract":["The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (\"inflammaging\"). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-α signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues prema"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["T cells with dysfunctional mitochondria induce multimorbidity and premature senescence."],"pmcid":["PMC7616968"],"funding_grant_id":["ERC-2016-StG 715322-EndoMitTalk","819775","2017-T2/BMD-5766","CP 19/014, PI16/188, PI19/00855","715322"],"pubmed_authors":["Ibanez B","Alcami A","Gortazar AR","Aranda JF","Alfranca A","Navarro MN","Hernaez B","Baixauli F","Desco M","Desdin-Mico G","Mittelbrunn M","Soto-Heredero G","Gabande-Rodriguez E","Cusso L","Carrasco E","Fernandez-Marcos P","Blanco EM","Oller J"],"additional_accession":[]},"is_claimable":false,"name":"T cells with dysfunctional mitochondria induce multimorbidity and premature senescence.","description":"The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (\"inflammaging\"). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-α signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues prema","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jun","modification":"2025-04-26T01:34:35.577Z","creation":"2025-04-06T10:14:43.325Z"},"accession":"S-EPMC7616968","cross_references":{"pubmed":["32439659"],"doi":["10.1126/science.aax0860"]}}